Dehydroepiandrosterone (DHEA) is an endogenous steroid hormone in higher primates, such as man, and is secreted by the adrenal glands, and possibly the testes. It is the most abundant steroid in humans, but no single specific receptor for DHEA has been identified. One of the main functions of DHEA is to act as a metabolic intermediate in the biosynthesis of androgens and estrogens. The serum levels of DHEA and its sulfated form, DHEA-S, peak in the early twenties and the levels then steadily decline beginning in the early thirties at a rate of about 5% per year. The decline in serum DHEA levels in both women and men is highly variable and the mechanism remains unknown.
DHEA and DHEA-S have been implicated in a number of biological processes such as a stimulatory effect on bone mineral density, a favorable effect on treating vaginal atrophy when applied locally, and control of muscle mass and strength, insulin sensitivity, and serum lipid levels. In the central nervous system (CNS), DHEA is recognized as a neurosteroid reaching the brain from systemic circulation. DHEA exerts its effects on the brain through multiple direct and indirect mechanisms. DHEA is believed to act directly with N-methyl-D-aspartate (NMDA) receptors, γ-aminobutyric acid (GABA) type A receptors and sigma receptors to regulate neuronal excitability. Further, DHEA can be metabolized in the CNS to both androgens and estrogens and modulate neuronal activity.
Although banned from use in athletic competitions as a pro-drug and a physician's prescription is required to obtain DHEA in some countries, the U.S. Food and Drug Administration currently considers DHEA to be a dietary supplement. As a dietary supplement, there is no regulation on the quantity, quality, or the purity of the DHEA in commercial formulations. Further, DHEA efficacy in treating medical conditions or diseases has not been completely elucidated, in part, because it exhibits poor solubility in aqueous solutions, rapid metabolism, and minimal oral bioavailability.